Autoimmune and Immune mediated skin diseases 3 Flashcards

Management of allergic skin disease, approach to pruritus

1
Q

What is the mechanism of action of lokivetmab (cytopoint)?

A

Monoclonal antibody therapy against IL-31. Blocks neuronal stimulation of pruritus by IL-31

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2
Q

Discuss the advantages of lokivetmab

A
  • Rapid onset of action
  • Injection only every 4 weeks
  • Can use in any age of dogs
  • can use in animals with impaired liver/kidney function and neoplasia
  • Can be used as an adjunctive treatment
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3
Q

What is a disadvantage of lokivetmab?

A

Minimal anti-inflammatory effect

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4
Q

Describe the mechanism of action of anti-histamines and evaluate their role in the treatment of AD

A
  • Block H1 histamine receptors of C neurones (+/- some central sedative effect)
  • Not very effective, but may allow reduction of dose of other drugs
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5
Q

State the licencing, and give examples of anti-histamines for dogs and cats

A
  • Not licensed in animals
  • Dogs: chlorpheniramine (piriton), hydroxyzine, cetirazine
  • Cats: chlorpheniramine, hydroxyzine
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6
Q

Describe the side effects of antihistamines

A
  • Rare, except drowsiness

- Care with cats, reported anorexia, vomiting, cardiac arrhythmias, excitability

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7
Q

What is the mechanism of action of tacrolimus?

A

Topical calcineurin inhibitor

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8
Q

Outline the advantages and disadvantages of tacrolimus in the treatment of AD

A
  • Minimal side effects
  • Can be beneficial for small hairless areas
  • But mild sting on applications and costly
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9
Q

How should Tacrolimus be administered?

A

Apply twice daily to alopecic area while wearing gloves

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10
Q

What is PEA-UM?

A

Palmitoylethanolamide-ultramicronised

- Recently release neutraceutical with EFAs/biotin, is a naturally occurring bioactive lipid

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11
Q

Evaluate the use of PEA-UM in the treatment of AD

A

Some efficacy shown in reducing pruritus/lesions in dogs with moderate CAD

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12
Q

What is allergen specific immunotherapy?

A

Immunotherapy vaccines made by selecting clinically relevant allergens, based on positive results from intradermal or serum IgE testing. Cannot be used for fleas or dietary allergens

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13
Q

What is the mode of action of allergen specific immunotherapy?

A

Exact mode unknown, but reduces allergen specific IgE and increases IL-10 and regulatory T cells

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14
Q

Describe the treatment protocol for allergen specific immnuotherapy

A
  • Subcut injection
  • Dosed every few days for 2 weeks, then increase gradually to maintenance, then given every 2-4 weeks
  • May be weaned off treatment but usually need maintenance injections monthly for life (can be given at home)
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15
Q

Discuss the efficacy of allergen specific immunotherapy

A
  • 25% can use as sole teatment
  • 40% helped but required other concurrent treatment
  • 25% ineffetive
  • Need up to 10-12 months to assess efficacy
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16
Q

What are the side effects of allergen specific immunotherapy?

A
  • Some increased pruritus for few days after injection
  • Rare anaphylaxis
  • Safe for long term use
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17
Q

Give an estimate of the cost of allergen specific immunotherapy

A

£300-400/year + vet’s fees

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18
Q

What is required in order to commence treatment for AD using allergen specific immunotherapy?

A

Not licensed in the UK so need informed consent from owner, and Special Import Certificate from VMD as is imported

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19
Q

Discuss the use of sublingual immunotherapy (SLIT) as a treatment for AD

A
  • Promising initial results
  • Twice daily administration long-term (difficult)
  • May be tolerated by animals that cannot tolerate injectable immunotherapy
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20
Q

What measures, additional to the main aspects of AD treatment, should be implemented in order to manage the condition?

A
  • Avoid flare factors such as ectoparasites, excessive heat/humidity and stress
  • Short term physical prevention of self trauma e.g. buster collars, coats, “soft claws”
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21
Q

Give an idea of the costs for the cheapest, standard and gold standard treatment for AD per year

A
  • Cheapest: steroid only, approx £90-165
  • Typical case treated by vet/dermatologist: £440-660
  • Treatment with ciclosporin (gold): 31300-6600
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22
Q

Outline the basic elements of a regime for the management and prevention of allergic skin disease

A
  • Use multiple treatments in combination
  • Warn owner of potential flare ups
  • Choose appropriate approach on individual basis
  • Tailor based on severity, speed of onset required, potential side effects, owner’s practical and financial constraints
  • Ongoing monitoring and adjustment required
  • Euthanasia is a valid option, esp. in cats (can cause serious damage to selves by scratching)
  • Anti-pruritic drugs if using immunotherapy while waiting for response
23
Q

List the differentials for an overweight GSD with a 4x5cm raised, alopecis plaque over left medial metatarsus, with an ulcerated surface and surrounding hyperpigmented halo

A
  • Acral lick granuloma
  • Neoplasia
  • Deep pyoderma
  • Fungal infection
  • Vasculitis
  • Atopy
  • Trauma
  • Foreign body
  • Demodicosis
  • Sterile pyogranuloma
24
Q

Define what is meant by acral lick granuloma

A

A skin disorder found commonly in dogs that develops from repetitive licking at the same area

25
Q

List the medical and stress triggers for acral lick dermatitis

A
  • Dermatological e.g. traumatic injury, infection, neoplasia, parasites
  • Allergy
  • Endocrine disease
  • Orthopaedic triggers (neoplasia, trauma, infection, joint pain, localised pain)
  • Neurological triggers (traumatic injury, spinal or nerve root neoplasia, lumbosacral degenerative stenosis, neuritis, congenital neurological disorders)
  • Stress
  • Fear, anxiety
  • Boredom
  • Attention seeking
26
Q

Explain how orthopaedic factors may trigger a true ALD

A

Pain will cause the dog to lick over the area

27
Q

Explain how neurological factors may trigger ALD

A

Cutaneous nerve damage may match an area of ALD, as well as congenital neurological disorders

28
Q

Outline a logical approach to the investigation of acral lick dermatitis

A
  • Identify lesion and perform impression smears, skin scrapes, hair pluck FNA
  • Then histopathology or tissue culture
  • Identify and treat underlying medical triggers
  • Treat infection based on culture results
  • Institute behavioural therapy: neuropharmacological drugs and behaviour modification
29
Q

Describe the typical findings on cytology of an ALD

A

Sterile inflammation with neutrophils and macrophages (indicating chronic process)

30
Q

Once a cytology sample has been taken from an ALD lesion, and identified as pyogranulomatous inflammation, what steps should be taken next?

A

Deep biopsy in order to examine for deep infection and histopathology. PAS staining for fungal hyphae and Ziehl-Neelsen staining for acid fast bacteria

31
Q

What are the main reasons for the common recurrence of ALD?

A
  • Failure to identify/address underlying cause
  • Failure to treat infection for long enough
  • Persistence of intradermal keratin/hair, provoking ongoing sterile inflammation even once infection has resolved
32
Q

What are the 2 classifications of pruritus?

A

Pruriceptive and neuropathic

33
Q

Define pruriceptive pruritus

A

Pruritus due to stimulation of periphera receptors in skin, in the presence of a healthy nervous system and usually due to skin disease

34
Q

Define neuropathic pruritus

A

Pruritus generated in CNS in response to circulation pruritogens (e.g. cholestasis), pharmacological mediators (e.g. intraspinal morphine), anatomical lesion of PNS or CNS (e.g. syringomyelia). Psychogenic pruritus recognised in man and animals. Nothing wrong witht the skin

35
Q

What are the 3 main groups of causes of pruritus?

A
  • Hypersensitivities
  • Parasites
  • Microbial infections
36
Q

Outline some “other” causes of pruritus

A
  • Contact irritants
  • Autoimmune conditions
  • Neoplasia
37
Q

When presented with a pruritic patient with Malassezia dermatitis, what diagnostic approach should be taken?

A
  • Malassezia dermatitis (and bacterial pyoderma) almost always secondary to an underlying cause
  • Need to identify and treat infection, and establish underlying cause
  • Clear secondary infection without corticosteroids and assess residual steroids
38
Q

What can be inferred if pruritus caused by Malassezia/ectoparasites/bacterial infection fully resolves with treatment (without corticosteroids)?

A
  • Either parasites and secondary infection had been present, need to continue parasite control in future
  • Potentially underlying immunosuppressive disease, including endocrinopathies
39
Q

What can be inferred if pruritus caused by Malassezia dermatitis remains following treatment for the Malassezia (without corticosteroids)?

A

Allergies and parasites if not controlled

40
Q

What diagnostic tests are required in the investigation of an animal presenting with pruritus?

A
  • Coat brushing/combing
  • Trichogram
  • Skin scrape
  • Cytology
  • Acetate tape strips
  • Wood’s lamp
  • Dermatophyte culture
41
Q

What is the first step in the clinical approach to an animal presenting with pruritus?

A
  • Get signalment and history
  • General and dermatological clinical exam
  • Decide on differentials and initial tests
42
Q

In a pruritic animal, following identification and treatment for parasites/bacterialMalassezia/dermatophyte infection, only a partial/no response has been noted. What steps would you take next?

A
  • Exclusion diet trial

- OR skin biopsy if suspicious of neoplasia/autoimmune disease

43
Q

In a pruritic animal, if there is no/only partial response to an exclusion diet trial, what would you do not?

A
  • Diagnose as atopic dermatitis

- OR skin biopsy if suspect neoplasia or autoimmune disease and not yet performed

44
Q

Give an example of a sex specific cause for pruritus

A

Sertoli cell tumours can cause secondary pyodermas in older male entire dogs

45
Q

What must be included in the history for a pruritic patient?

A
  • Age of onset
  • Areas affected
  • Opportunity for contagion
  • Evidence of contagion/zoonotic disease
  • Signs of systemic disease
46
Q

When you have formed a differentials list for a pruritic patient, which differentials should you aim to rule in/out first? How?

A
  • Ectoparasites and microbial infection
  • Avoid use of glucocorticoids
  • Use coat brushings, tape strips, trichograms, skin scrapes etc.
  • Skin surface cytology, Wood’s lamp
47
Q

Once a bacterial or Malassezia infection has been identified on cytology, how should you procede?

A
  • treat appropriately to eliminate
  • Bacterial: topical chlorhexidine, 3 week course of suitable antibiotics
  • Malassezia: miconazole/chlorhexidine wash 2-3x weekly
48
Q

Why should glucocorticoid treatment be avoided initially in a pruritic patient?

A
  • Interfere with diagnostic testing e.g. skin biopsy, blood tests
  • Can create dermatological side effects e.g. secondary pyoderma
  • Alters lesion appearance
  • May preclude assessment of efficacy of other treatment
  • Potential systemic side effects
49
Q

Describe the common signalment and history for sarcoptic mange

A
  • Any age of onset

- Fox contact increases risk

50
Q

Describe the clinical signs of sarcoptic mange

A
  • Pruritus, papules, crusts

- Affecting in particular (but not exclusively) pinnal margins, hocks, lateral elbows, ventrum

51
Q

Describe the signalment and signs of Neotrombiculosis

A
  • Often seasonal, June-Sept

- Often feet (interdigital skin) and head affected

52
Q

Describe the signalment of hookworms

A

Often kennelled dogs, unsanitary conditions, unlikely if wormed

53
Q

Describe the clinical signs of Pelodora (hookworms)

A
  • Affects skin in contact with ground (feet, ventrum)

- +/- GI signs (are GI worms that enter through skin)

54
Q

Outline a treatment plan for an animal with atopic dermatitis and Malassezia dermatitis, where the owner has financial restraints

A
  • Treat Malassezia using topical or systemic antifungals e.g. miconazole/chlorhexidine washes/sprays foams
  • Treat AD using glucocorticoids (oral and topical can be used), care re. iatrogenic Cushing’s
  • Antihistamines (but not necessarily only as good as the placebo…)